SvO2
2
In a study of patients with sepsis, Velissaris and colleagues showed that high mixed venous blood oxygen saturation (SvO 2 ) levels do not exclude fluid responsiveness [1]. SvO 2 is assumed to reflect the balance between arterial oxygen delivery (DO 2 ) and oxygen consumption (VO 2 ) provided arterial blood oxygen saturation (SaO 2 ) is normal. Indeed, the modified Fick equation states: SvO 2 = SaO 2 – [VO 2 / (cardiac output × Hb × 1.34)] where Hb is the hemoglobin concentration. Nevertheless, the interpretation of SvO 2 and its changes in shock states must be cautious for at least four reasons. First, in any shock state, oxygen demand exceeds VO 2 by definition such that SvO 2 cannot reflect the balance between DO 2 and oxygen demand, which is better assessed by markers of anaerobic metabolism such as the blood lactate level. Second, as VO 2 /DO 2 dependency is a characteristic pattern of shock states [2], any increase in DO 2 during resuscitation will be associated with a simultaneous increase in VO 2 and hence with no or only a small increase in SvO 2 until a critical DO 2 is reached. ird, the tissue oxygen utiliza- tion is impaired in severe sepsis so VO 2 may decrease relative to oxygen demand, even if DO 2 is normal or high. Fourth, because of the hyperbolic relationship between SvO 2 and cardiac output (graphical represen- tation of the modified Fick equation) [3], SvO 2 should not change much in response to an increase in cardiac output in cases of hyperdynamic shock states. For all these reasons, interest in SvO 2 monitoring in septic shock has been debated – although SvO 2 or its surro- gate, central venous oxygen saturation, has been recom- mended as a major hemodynamic target of early resuscitation in septic shock [4,5]. Nevertheless, SvO 2 might still play an important role in the monitoring of septic shock by identifying the patients in whom DO 2 could be further augmented and then by guiding the therapy aimed at increasing DO 2 . is point is of particular importance since systematic maximization of DO 2 is not recommended in every patient with septic shock [5]. Velissaris and colleagues showed that a given value of SvO 2 cannot be used to predict a positive response to fluid challenge [1]. ese results are quite consistent with the basic physiology and deserve to be discussed. Preload responsiveness is an intrinsic property of cardiac performance, indicating that the heart is operating on the steep ascending part of the Frank–Starling relationship [6]. Preload responsiveness is therefore by nature a concept that differs from the concept of global VO 2 /DO 2 balance and thus from SvO 2 . Abstract Real-time monitoring of mixed venous oxygen blood saturation (SvO 2 ) or of central venous oxygen blood saturation is often used during resuscitation of septic shock. However, the meaning of these parameters is far from straightforward. In the present commentary, we emphasize that SvO 2 – a global marker of tissue oxygen balance – can never be simplistically used as a marker of preload responsiveness, which is an intrinsic marker of cardiac performance. In some septic shock patients, because of profound hypovolemia or myocardial dysfunction, SvO 2 can be low but obviously cannot alone indicate whether a fluid challenge would increase cardiac output. In other patients, because of a profound impairment of oxygen extraction capacities, SvO 2 can be abnormally high even in patients who are still able to respond positively to fluid infusion. In any case, other reliable dynamic parameters can help to address the important question of fluid responsiveness/unresponsiveness. However, whether fluid administration in fluid responders and high SvO 2 would be efficacious to reduce tissue dysoxia in the most injured tissues is still uncertain. SvO 2 to monitor resuscitation of septic patients: let’s just understand the basic physiology Jean-Louis Teboul 1,2 *, Olfa Hamzaoui 3 and Xavier Monnet 1,2 See related research by Velissaris et al ., http://ccforum.com/content/15/4/R177 COMMENTARY *Correspondence: [email protected] 1 Service de Réanimation Médicale, Hôpital de Bicêtre, Hôpitaux Universitaires Paris-Sud, 78 rue du Général Leclerc, 94 270 Le Kremlin-Bicêtre, France Full list of author information is available at the end of the article Teboul et al. Critical Care 2011, 15:1005 http://ccforum.com/content/15/6/1005 © 2011 BioMed Central Ltd
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SvO2
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In a study of patients with sepsis, Velissaris and colleagues showed that high mixed venous blood oxygen saturation (SvO2) levels do not exclude uid responsiveness [1]. SvO2 is assumed to re ect the balance between arterial oxygen delivery (DO2) and oxygen consumption (VO2) provided arterial blood oxygen saturation (SaO2) is normal. Indeed, the modi ed Fick equation states:
SvO2 = SaO2 [VO2 / (cardiac output Hb 1.34)]
where Hb is the hemoglobin concentration.Nevertheless, the interpretation of SvO2 and its
changes in shock states must be cautious for at least four reasons. First, in any shock state, oxygen demand exceeds VO2 by de nition such that SvO2 cannot re ect the balance between DO2 and oxygen demand, which is better assessed by markers of anaerobic metabolism such as the blood lactate level. Second, as VO2/DO2dependency is a characteristic pattern of shock states [2], any increase in DO2 during resuscitation will be associated with a simul taneous increase in VO2 and hence with no or only a small increase in SvO2 until a critical DO2 is reached. Th ird, the tissue oxygen utiliza-tion is impaired in severe sepsis so VO2 may decrease relative to oxygen demand, even if DO2 is normal or high. Fourth, because of the hyperbolic relation ship between SvO2 and cardiac output (graphical represen-tation of the modi ed Fick equation) [3], SvO2 should not change much in response to an increase in cardiac output in cases of hyperdynamic shock states. For all these reasons, interest in SvO2 monitoring in septic shock has been debated although SvO2 or its surro-gate, central venous oxygen saturation, has been recom-mended as a major hemodynamic target of early resuscitation in septic shock [4,5].
Nevertheless, SvO2 might still play an important role in the monitoring of septic shock by identifying the patients in whom DO2 could be further augmented and then by guiding the therapy aimed at increasing DO2. Th is point is of particular importance since systematic maximization of DO2 is not recommended in every patient with septic shock [5].
Velissaris and colleagues showed that a given value of SvO2 cannot be used to predict a positive response to uid challenge [1]. Th ese results are quite consistent with the basic physiology and deserve to be discussed. Preload responsiveness is an intrinsic property of cardiac performance, indicating that the heart is operating on the steep ascending part of the FrankStarling relationship [6]. Preload responsiveness is therefore by nature a concept that di ers from the concept of global VO2/DO2balance and thus from SvO2.
AbstractReal-time monitoring of mixed venous oxygen blood saturation (SvO2) or of central venous oxygen blood saturation is often used during resuscitation of septic shock. However, the meaning of these parameters is far from straightforward. In the present commentary, we emphasize that SvO2 a global marker of tissue oxygen balance can never be simplistically used as a marker of preload responsiveness, which is an intrinsic marker of cardiac performance. In some septic shock patients, because of profound hypovolemia or myocardial dysfunction, SvO2 can be low but obviously cannot alone indicate whether a fl uid challenge would increase cardiac output. In other patients, because of a profound impairment of oxygen extraction capacities, SvO2 can be abnormally high even in patients who are still able to respond positively to fl uid infusion. In any case, other reliable dynamic parameters can help to address the important question of fl uid responsiveness/unresponsiveness. However, whether fl uid administration in fl uid responders and high SvO2 would be effi cacious to reduce tissue dysoxia in the most injured tissues is still uncertain.
2010 BioMed Central Ltd
SvO2 to monitor resuscitation of septic patients: lets just understand the basic physiologyJean-Louis Teboul1,2*, Olfa Hamzaoui3 and Xavier Monnet1,2
See related research by Velissaris et al., http://ccforum.com/content/15/4/R177
COMMENTARY
*Correspondence: [email protected] de Ranimation Mdicale, Hpital de Bictre, Hpitaux Universitaires Paris-Sud, 78 rue du Gnral Leclerc, 94 270 Le Kremlin-Bictre, FranceFull list of author information is available at the end of the article
Teboul et al. Critical Care 2011, 15:1005 http://ccforum.com/content/15/6/1005
2011 BioMed Central Ltd
-
Patients with low SvO2 can be either uid responsive in cases of hypovolemic shock or uid unresponsive in cases of cardiogenic shock. In the study by Velissaris and colleagues almost two-thirds of patients with a low SvO2 (70%) at baseline [1]. Th is con rms that preload responsiveness can coexist with the presence of reduced oxygen extraction capacities and thus high SvO2. A reliable prediction of uid responsiveness would also be important to obtain in cases of high SvO2. Whether the presence of preload responsiveness should lead to the decision to infuse uid, however, is still uncertain. One should anticipate that abnormally high SvO2 is an indicator of profoundly decreased oxygen extraction capacities so that the additional increase in DO2 cannot be e ectively distri-buted and/or utilized in the most injured peripheral tissues. In other words, one can reasonably postulate in cases of tissue hypoxia that the higher the SvO2, the less likely the correction of tissue hypoxia with uid infusion, even in the presence of indicators of preload responsive-ness. Since the study by Velissaris and colleagues [1] was not designed to con rm this hypothesis, further studies are required.
AbbreviationsDO2, oxygen delivery; Hb, hemoglobin concentration; SaO2, arterial blood oxygen saturation; SvO2, mixed venous blood oxygen saturation; VO2, oxygen consumption.
Competing interestsJ-LT and XM are members of the Medical Advisory Board of Pulsion Medical Systems (Munich, Germany). OH declares that he has no competing interests.
Author details1Service de Ranimation Mdicale, Hpital de Bictre, Hpitaux Universitaires Paris-Sud, 78 rue du Gnral Leclerc, 94270 Le Kremlin-Bictre, France. 2Facult de Mdecine Paris-Sud, Universit Paris-Sud, EA 4046, 63 rue Gabriel Pri, 94270 Le Kremlin-Bictre, France. 3Service de Ranimation Mdicale, Hpital Antoine Bclre, Hpitaux Universitaires Paris-Sud, 157 rue de la Porte des Trivaux, 92141 Clamart, France.
Published: 7 November 2011
References1. Velissaris D, Pierrakos C, Scolletta S, De Backer D, Vincent JL: High mixed
venous oxygen saturation levels do not exclude fl uid responsiveness in critically ill septic patients. Crit Care 2011, 15:R177.
2. Schumacker PT, Cain SM: The concept of a critical oxygen delivery. Intensive Care Med 1987, 13:223-229.
3. Jain A, Shroff SG, Janicki JS Reddy HK, Weber KT: Relation between mixed venous oxygen saturation and cardiac index. Nonlinearity and normalization for oxygen uptake and hemoglobin. Chest 1991, 99:1403-1409.
4. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M; Early Goal-Directed Therapy Collaborative Group: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001, 345:1368-1377.
5. Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, Reinhart K, Angus DC, Brun-Buisson C, Beale R, Calandra T, Dhainaut JF, Gerlach H, Harvey M, Marini JJ, Marshall J, Ranieri M, Ramsay G, Sevransky J, Thompson BT, Townsend S, Vender JS, Zimmerman JL, Vincent JL: Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med 2008, 34:17-60.
6. Monnet X, Teboul JL: Volume responsiveness. Curr Opin Crit Care 2007, 13:549-553.
7. Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL: Cardiac fi lling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med 2007, 35:64-68.
8. Marik PE, Monnet X, Teboul JL: Hemodynamic parameters to guide fl uid therapy. Annals Intensive Care 2011, 1:1.
9. Teboul JL, Monnet X: Detecting volume responsiveness and unresponsiveness in intensive care unit patients: two diff erent problems, only one solution. Crit Care 2009, 13:175.
10. Kraft P, Steltzer H, Hiesmayr M, Klimscha W, Hammerle AF: Mixed venous oxygen saturation in critically ill septic shock patients. The role of defi ned events. Chest 1993, 103:900-906.
11. van Beest PA, Hofstra JJ, Schultz MJ, Boerma EC, Spronk PE, Kuiper MA: The incidence of low venous oxygen saturation on admission to the intensive care unit: a multi-center observational study in The Netherlands. Crit Care 2008, 12:R33.
doi:10.1186/cc10491Cite this article as: Teboul JL, et al.: SvO2 to monitor resuscitation of septic patients: lets just understand the basic physiology. Critical Care 2011, 15:1005.
Teboul et al. Critical Care 2011, 15:1005 http://ccforum.com/content/15/6/1005
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